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Medicine (Baltimore) ; 98(44): e17751, 2019 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-31689830


Maternal bacterial sepsis during pregnancy and the postpartum period is a common cause of maternal mortality and fetal morbidity and mortality. This study was performed to analyze perinatal prognosis and related factors of maternal bacterial sepsis in west China.We conducted a cross-sectional study of pregnant women with bacterial sepsis who were admitted into a tertiary care center in western China between 2011and 2015. Data from these cases were collected and analyzed.Eighty six women were identified with bacterial sepsis in our hospital, and the incidence of maternal bacterial sepsis was 1.7 per 1000 maternities, the incidence of septic shock was 1.8 per 10,000 maternities, and 1 maternal death occurred. Among the 86 pregnant women with bacterial sepsis, genital tract infection was the most common source of infection (41/86, 47.7%). The most common bacteria in the Gram-positive bacteria group was Listeria monocytogenes and in the Gram-negative bacteria group was Escherichia coli. The premature delivery rate (65.7%) was substantially higher in the Gram-negative bacteria group (P = .011), and the miscarriage rate (31.3%) was higher in the Gram-positive bacteria group (P = .042). The fetal/neonatal mortality rate was 20% (21/105) and higher in the Gram-positive bacteria group (P = .008), and the infant mortality rate in 1 year was 7.1% (6/84).Bacterial sepsis remains an alarming cause of both maternal and fetal morbidity and mortality, and infant mortality. Key treatment involves a multi-disciplinary group of clinicians with experience in all aspects of the care of pregnant women with sepsis and early initiation of appropriate antibiotics according to the type of bacterial infection. The effect of maternal sepsis on long-term fetal outcome should be investigated.

Bactérias Gram-Negativas , Bactérias Gram-Positivas , Complicações Infecciosas na Gravidez/mortalidade , Infecções do Sistema Genital/mortalidade , Sepse/mortalidade , Aborto Espontâneo/microbiologia , Aborto Espontâneo/mortalidade , Adulto , China/epidemiologia , Estudos Transversais , Feminino , Humanos , Incidência , Lactente , Mortalidade Infantil , Recém-Nascido , Mortalidade Materna , Gravidez , Complicações Infecciosas na Gravidez/microbiologia , Infecções do Sistema Genital/microbiologia , Sepse/microbiologia
Infect Immun ; 86(7)2018 07.
Artigo em Inglês | MEDLINE | ID: mdl-29661927


CD4 T cells and antibody are required for optimal acquired immunity to Chlamydia muridarum genital tract infection, and T cell-mediated gamma interferon (IFN-γ) production is necessary to clear infection in the absence of humoral immunity. However, the role of T cell-independent immune responses during primary infection remains unclear. We investigated this question by inoculating wild-type and immune-deficient mice with C. muridarum CM001, a clonal isolate capable of enhanced extragenital replication. Genital inoculation of wild-type mice resulted in transient dissemination to the lungs and spleen that then was rapidly cleared from these organs. However, CM001 genital infection proved lethal for STAT1-/- and IFNG-/- mice, in which IFN-γ signaling was absent, and for Rag1-/- mice, which lacked T and B cells and in which innate IFN-γ signaling was retained. In contrast, B cell-deficient muMT mice, which can generate a Th1 response, and T cell-deficient mice with intact B cell and innate IFN-γ signaling survived. These data collectively indicate that IFN-γ prevents lethal CM001 dissemination in the absence of T cells and suggests a B cell corequirement. Adoptive transfer of convalescent-phase immune serum but not naive IgM to Rag1-/- mice infected with CM001 significantly increased the survival time, while transfer of naive B cells completely rescued Rag1-/- mice from CM001 lethality. Protection was associated with a significant reduction in the lung chlamydial burden of genitally infected mice. These data reveal an important cooperation between T cell-independent B cell responses and innate IFN-γ in chlamydial host defense and suggest that interactions between T cell-independent antibody and IFN-γ are essential for limiting extragenital dissemination.

Linfócitos B/imunologia , Infecções por Chlamydia/imunologia , Chlamydia muridarum , Interferon gama/imunologia , Infecções do Sistema Genital/imunologia , Linfócitos T/fisiologia , Animais , Infecções por Chlamydia/mortalidade , Chlamydia muridarum/genética , Feminino , Proteínas de Homeodomínio/fisiologia , Camundongos , Camundongos Endogâmicos C57BL , Plasmídeos , Infecções do Sistema Genital/mortalidade